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Submit ReviewCP 31398 dihydrochloride is a p53 stabilizing agent. Stabilizes the active conformation of p53 and promotes p53 activity in cancer cell lines with mutant or wild-type p53. Inhibits growth of small human tumor xenografts in vivo.
Sold for research purposes under agreement from Pfizer Inc.
M. Wt | 435.39 |
Formula | C22H26N4O.2HCl |
Storage | Desiccate at RT |
Purity | ≥99% (HPLC) |
CAS Number | 1217195-61-3 |
PubChem ID | 56972205 |
InChI Key | WWIFDJIOGCGSBS-IVKCLRODSA-N |
Smiles | COC(C=C3)=CC=C3/C=C/C2=NC1=CC=CC=C1C(NCCCN(C)C)=N2.Cl.Cl |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
References are publications that support the biological activity of the product.
Foster et al (1999) Pharmacological rescue of mutant p53 conformation and function. Science 286 2507 PMID: 10617466
Wischhusen et al (2003) CP-31398, a novel p53-stabilizing agent, induces p53-dependent and p53-independent glioma cell death. Oncogene 22 8233 PMID: 14614447
Demma et al (2004) CP-31398 restores DNA-binding activity to mutant p53 in vitro but does not affect p53 homologs p63 and p73. J.Biol.Chem. 279 45887 PMID: 15308639
Keywords: CP 31398 dihydrochloride, CP 31398 dihydrochloride supplier, p53-stabilizing, p53-stabilising, agent, Transcription, Factors, CP31398, dihydrochloride, Pfizer, p53, 3023, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for CP 31398 dihydrochloride include:
Grugan et al (2013) A common p53 mutation (R175H) activates c-Met receptor tyrosine kinase to enhance tumor cell invasion. Mol Cell Neurosci 14 853 PMID: 23792586
Roh et al (2011) p53-Reactivating small molecules induce apoptosis and enhance chemotherapeutic cytotoxicity in head and neck squamous cell carcinoma. Oral Oncol 47 8 PMID: 21109480
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This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 products, including research tools for:
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. This poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.